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    Home > Active Ingredient News > Endocrine System > [Yao's Anesthesiology] Thyrotoxicosis (1)

    [Yao's Anesthesiology] Thyrotoxicosis (1)

    • Last Update: 2022-01-10
    • Source: Internet
    • Author: User
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    Thyrotoxicosis patient, male, 48 years old, diffuse neck enlargement
    .

    History of present illness: significant dyspnea, dysphagia, weight loss, paroxysmal palpitations and heat intolerance
    .

    The blood pressure is 160/100 mmHg, the heart rate is 120 beats/min, and the hematocrit is 29%
    .

    A.
    Disease status and differential diagnosis 1.
    What is the diagnosis consistent with these symptoms? 2.
    Describe the synthesis, release and peripheral transformation of tetraiodothyronine (T4) and triiodothyronine (T3)
    .

    3.
    What is the role of the hypothalamic-pituitary axis in thyroid function? 4.
    The role of thyroid hormones
    .

    5.
    What is the cause of hyperthyroidism? 6.
    What are the clinical symptoms and signs of thyrotoxicosis? 7.
    How to distinguish thyroid crisis and thyrotoxicosis? 8.
    What are the causes of thyroid crisis? 9.
    What are the innervations of the larynx? B.
    Preoperative evaluation and preparation 1.
    Will an enlarged thyroid cause local anatomical changes? 2.
    Describe the symptoms and signs of superior vena cava compression syndrome
    .

    3.
    How to evaluate airway blockage? 4.
    What are the laboratory tests to check thyroid function? 5.
    A treatment plan to restore thyroid function to normal
    .

    6.
    What are the benefits of adrenergic block? 7.
    When can patients with hyperthyroidism undergo elective surgery? 8.
    How do patients with hyperthyroidism give preoperative medication? 9.
    How to prepare for emergency surgery for patients with thyrotoxicosis? Partial breakdown A.
    Disease conditions and differential diagnosis A.
    1.
    What is the diagnosis consistent with these symptoms? These symptoms and signs are typical manifestations of hyperthyroidism
    .

    Differential diagnosis includes other hypermetabolic states: such as pheochromocytoma, carcinoid, chronic infection, anxiety state, fatal catatonia, exercise heatstroke and certain drugs such as inhaled anesthetics, sympathomimetic drugs, serotonin antagonists , Antipsychotic drugs and other drugs with anticholinergic effects
    .

    A2.
    Describe the synthesis, release and peripheral transformation of tetraiodothyronine (T4) and triiodothyronine (T3)
    .

    The synthesis of thyroid hormone requires iodine
    .

    The source of iodine is food intake or deiodination of existing thyroid hormones
    .

    Iodine is actively transported to thyroid cells and accumulates in the form of iodide
    .

    Iodine combines with the tyrosine residues on thyroglobulin (iodine receptor protein) to organize iodine
    .

    The iodinated tyrosine residues are coupled to exist in the form of T4 and T3
    .

    Under the regulation of thyroid stimulating hormone, once thyroid hormone is cleaved from thyroglobulin, it is released into the circulation
    .

    90% of the hormones secreted by the thyroid are T4 and only 10% are T3.
    T3 is biologically active but has a short half-life
    .

    In peripheral tissues, most of T4 is transformed into T3
    .

    T4 can also be converted into the inactive metabolite reverse T3
    .

    In the circulation, most of the T4 and T3 are bound to plasma proteins (mainly thyroid hormone binding globulin), a small part is bound to albumin and prealbumin, and less than 1% of the hormones are present in the plasma in a free form
    .

    A3.
    What is the role of the hypothalamic-pituitary axis in thyroid function? The hypothalamus secretes thyrotropin-releasing hormone (TRH), which then stimulates the synthesis and release of thyroid-stimulating hormone (TSH) in the anterior pituitary gland
    .

    TSH stimulates the thyroid gland to synthesize and secrete thyroxine
    .

    In the pituitary cells, T4 is transformed into T3, and the level of T3 in the pituitary cells regulates the release of TSH from the pituitary
    .

    A low concentration of T3 stimulates the release of TSH, while a high level of thyroid hormone concentration inhibits the secretion of TSH
    .

    A4.
    The role of thyroid hormones
    .

    Thyroid hormones work at the cellular level, organ level, and systemic level
    .

    Effects on organs•Thyroid hormone has a direct effect on the heart, increasing heart rate and myocardial contractility, thereby increasing cardiac output
    .

    • Thyroid hormones increase oxygen consumption and carbon dioxide production, thereby compensatoryly increasing respiratory rate and tidal volume
    .

    • Thyroid hormones increase bone formation and catabolism, thereby changing parathyroid hormone levels
    .

    Effects on the whole body•Thyroid hormones increase cell metabolism and increase the production of metabolic end products, which leads to vasodilation and increased tissue blood perfusion
    .

    A5.
    What is the cause of hyperthyroidism? The main cause of hyperthyroidism (hyperthyroidism) is Graves disease, which accounts for 90% of the total cases
    .

    Thyroiditis is the second most common cause
    .

    Other less common causes, such as multinodular toxic goiter, single toxic thyroid nodule, excessive consumption of exogenous iodide, and the side effects of certain drug treatments can all cause hyperthyroidism
    .

    Hyperthyroidism caused by trophoblastic tumors (such as hydatidiform mole and choriocarcinoma) is rare
    .

    A6.
    What are the clinical symptoms and signs of thyrotoxicosis? The severity of thyrotoxicosis, the duration of the disease, the patient's susceptibility to excessive thyroid hormones, and the patient's age determine the patient's clinical symptoms
    .

    Non-specific symptoms such as hyperhidrosis, heat intolerance, weakness, and insomnia are common symptoms and signs of thyrotoxicosis
    .

    Due to the increase in metabolic rate, the patient will lose weight regardless of whether the patient's appetite is normal or increased
    .

    Tremors and eyelid retraction often occur, resulting in reduced blinking, which are the result of sympathetic overexcitement
    .

    Thyrotoxicosis also significantly affects the cardiovascular system, leading to increased cardiovascular morbidity and mortality.
    The main causes of death are heart failure and thromboembolism
    .

    The cardiovascular system changes in thyrotoxicosis include tachycardia, increased stroke volume, increased cardiac output, increased oxygen consumption, and decreased systemic and pulmonary vascular resistance
    .

    In addition, patients also showed increased myocardial contractility, autonomy, and irritability
    .

    The pulse pressure increases with the increase in systolic blood pressure
    .

    Patients with coronary atherosclerosis may induce or aggravate angina pectoris
    .

    Young adult patients can usually tolerate hyperthyroidism without cardiovascular decompensation
    .

    Elderly patients and patients whose hearts have been damaged may suffer from high cardiac output congestive heart failure
    .

    Patients with thyrotoxicosis may also present with sinus tachycardia, atrial fibrillation, complete heart block, and ventricular arrhythmia
    .

    Hypercapnia and increased oxygen consumption caused by hypermetabolism compensatoryly increase minute ventilation, shortness of breath, and increase in tidal volume
    .

    Due to weakened muscle strength and decreased lung compliance, lung capacity is reduced, but lung diffusion capacity remains normal
    .

    During exercise, ventilation and oxygen intake increase
    .

    Nervous system manifestations include anxiety, irritability, tremor, insomnia, muscle weakness, and cognitive dysfunction, such as confusion and delirium
    .

    Severe patients can progress to stupor, dullness or even coma
    .

    Other manifestations include myopathy, periodic paralysis, seizures, chorea, and tremor at rest
    .

    It can be expressed as a fast wave increase on the EEG
    .

    Thyrotoxicosis shortens the emptying time of the gastrointestinal tract and may cause secretory diarrhea
    .

    Weight loss often occurs due to increased demand for calories
    .

    Gastric acid secretion is sometimes reduced (30% of patients have parietal cell antibodies), which may affect drug absorption
    .

    Abnormalities of the blood system include anemia, neutropenia, and thrombocytopenia
    .

    As the oxygen requirement increases, the number of red blood cells increases
    .

    The effect on the kidneys increases renal tubular reabsorption and secretion, which ultimately leads to a decrease in potassium excretion and an increase in sodium excretion
    .

    A7.
    How to distinguish between thyroid crisis and thyrotoxicosis? Thyrotoxicosis refers to the dysfunction of all organs of the body caused by the increase in the concentration of thyroid hormone
    .

    The clinical symptoms are different, and the mild ones are biochemical abnormalities without clinical symptoms
    .

    In severe cases, multiple organ dysfunction may be life-threatening and high mortality
    .

    Thyroid crisis often occurs when the patient's metabolism, body temperature regulation, and cardiovascular system decompensation
    .

    Thyroid crisis has the following 4 main characteristics: fever, tachycardia or supraventricular arrhythmia, central nervous system symptoms and gastrointestinal symptoms
    .

    Early detection and aggressive treatment can reduce morbidity and mortality
    .

    There is no laboratory test to distinguish thyroid crisis from thyrotoxicosis
    .

    Need to perform thyroid function test
    .

    Therefore, once a thyroid crisis is suspected, active treatment should be started immediately, and treatment should not be delayed due to waiting for the test results
    .

    The goals of treatment are: reduce the level of thyroid hormones in the circulation; inhibit the effects of thyroid hormones in the circulation on peripheral tissues; support treatment and remove incentives
    .

    A8.
    What are the causes of thyroid crisis? Thyroid crisis occurs suddenly.
    The following conditions that cause a rapid increase in the level of thyroid hormones are the cause of the thyroid crisis, such as thyroid surgery, cessation of antithyroid drug treatment, radioactive iodine therapy, lipiodol contrast examination, and rough thyroid examination Check operation
    .

    Non-thyroid related triggers include: non-thyroid surgery, infection, cerebrovascular accident, congestive heart failure, intestinal obstruction, pulmonary embolism, pregnancy, childbirth, diabetic ketoacidosis, trauma, or certain iodine-containing drugs (amiodarone ) Application may also induce thyroid crisis
    .

    The induction of thyroid crisis is mainly related to the drastic changes in the level of thyroid hormone, rather than the absolute level of thyroid hormone
    .

    A9.
    What are the innervations of the larynx? The larynx is innervated by two branches of the vagus nerve: the superior laryngeal nerve and the recurrent laryngeal nerve
    .

    The superior laryngeal nerve is divided into two branches, the inner branch enters the larynx through the thyrohyoid periosteum (the sensory and autonomic nerve branch), and the outer branch is outside the larynx (the motor nerve branch)
    .

    The inner laryngeal nerve branch passes through the thyrohyoid periosteum and controls the sensation of the larynx above the vocal cords
    .

    The outer branches are distributed on the surface of the thyrohyoid periosteum, innervating the cricothyroid muscle and part of the transverse dipper muscle
    .

    The recurrent laryngeal nerve innervates the movement of all muscles in the larynx and the sensation of the larynx below the vocal cords
    .

    The cricothyroid muscle is the only tensor muscle of the larynx
    .

    Bilateral recurrent laryngeal nerve injury will cause paralysis of all muscles in the larynx except for the cricothyroid muscle and part of the transverse dipper muscle
    .

    The vocal cords are near the middle position, causing airway obstruction
    .

    However, the vocal cords are not tense at this time, but in a relaxed state
    .

    This is because the cricothyroid needs other muscles in the larynx to keep the vocal cords tight
    .

    When a unilateral recurrent laryngeal nerve is injured, the injured side of the vocal cord is in a neutral position, while the other side of the vocal cord remains normal
    .

    Among complications, hoarseness and aspiration are more common than airway obstruction
    .

    B.
    Preoperative evaluation and preparation Bl.
    Will an enlarged thyroid cause local anatomical changes? The thyroid gland does not completely surround the trachea and esophagus
    .

    Enlarged glands can cause compression symptoms of the trachea and esophagus, such as dyspnea and dysphagia
    .

    Whether the anatomical location of the gland is on the breastbone or below the breastbone, the symptoms caused are significantly different
    .

    Airway involvement includes: airway displacement, airway compression, and lumen stenosis
    .

    If the respiratory muscle tension disappears with medication, once the muscles relax, the enlarged thyroid gland located under the breastbone may cause unexpected airway compression
    .

    Airway infiltration or bleeding in the airway can be seen in patients with thyroid cancer
    .

    Due to its anatomical position, the superior vena cava in the thoracic cavity is easily compressed by mediastinal tumors
    .

    It is reported that patients with retrosternal goiter may also experience bilateral vocal cord paralysis due to compression of the recurrent laryngeal nerve, and secondary acute respiratory insufficiency
    .

    B2.
    Describe the symptoms and signs of superior vena cava compression syndrome
    .

    Superior vena cava compression syndrome is the result of chronic and insidious gradual compression/occlusion of the superior vena cava
    .

    The superior vena cava has small blood flow, low pressure, and thin tube wall, which makes it easy to be oppressed by enlarged mediastinal tumors
    .

    Low intraluminal pressure can easily lead to thrombosis, such as those caused by intravenous catheters
    .

    Obstruction of venous return leads to the formation of interstitial edema and collateral circulation, causing edema of the face, neck and upper limbs, collateral varicose veins in the neck and upper chest, headache and dizziness
    .

    Since the right thyroid is relatively larger than the left, compression of the unnamed vein on the right is more common
    .

    Compression of the superior vena cava will form a wide range of collateral circulation such as the odd venous plexus, internal breast venous plexus, spinal venous plexus, and lateral thoracic venous plexus
    .

    Venography is the "gold standard" for describing these anatomical changes
    .

    B3.
    How to evaluate airway obstruction? Chest radiograph and neck CT can help assess the position of the trachea and the degree of airway blockage
    .

    Pulmonary function test is a non-invasive method used to assess the degree of airway blockage in patients
    .

    Flow rate-volume curve analysis can determine the degree and location of airway blockage
    .

    The flow rate-volume curve is a circular curve obtained by inhaling hard to the total lung volume, then exhaling to the residual volume, and then inhaling to the total lung volume
    .

    The different shapes of the flow-volume curve can help distinguish intrathoracic and extrathoracic airway obstruction (see Figure 1) o Fixed upper respiratory tract lesions, including airway tumors, subglottic stenosis and goiter, in the flow-volume curve.
    There will be a plateau in both the gas phase and the expiratory phase (see Figure 1A).
    Variable chest lesions are usually caused by vocal cord paralysis, vocal cord neoplasms, and neck neoplasms
    .

    A plateau appears in the inspiratory phase of the flow rate-volume curve
    .

    When inhaling, the negative pressure inside the chest is generated to close the airway outside the chest
    .

    When exhaling, the airflow keeps the airway open (see Figure 1B)
    .

    Variable intrathoracic airway diseases include intrabronchial tumors, tracheal tumors and tracheomalacia, which only cause a plateau in the expiratory phase of the flow rate-volume curve
    .

    When inhaling, the negative pressure in the chest keeps the airway open, so the inspiratory phase is not affected
    .

    During exhalation, positive intrathoracic pressure narrows the airway, and a plateau appears in the expiratory phase of the flow-volume loop (see Figure 1C)
    .

    The forced vital capacity of these patients remained normal, but the forced expiratory volume in the first second was significantly reduced
    .

    B4.
    What are the laboratory tests to check thyroid function? B5.
    Treatment plan to restore thyroid function to normal
    .

    There are three methods of drug treatment: directly inhibit the production of thyroid hormone, inhibit the release of thyroid hormone, and control the adrenergic effect caused by excessive thyroid hormone
    .

    The initial treatment is mainly to use antithyroid drugs to inhibit the synthesis of thyroid hormones, such as methimidine and propylthiouracil
    .

    Such drugs are not effective on the synthesized thyroid hormones, and they cannot be fully effective until the synthesized hormones are consumed
    .

    Propylthiouracil also has the effect of inhibiting the conversion of T4 to T3 in peripheral tissues
    .

    Side effects of antithyroid drugs include fever, urticaria, joint pain, arthritis, leukopenia, agranulocytosis, and, more rarely, toxic hepatitis
    .

    Glucocorticoids inhibit the conversion of T4 to T3 in peripheral tissues, and have a synergistic effect when used together with propylthiouracil
    .

    After treatment with antithyroid drugs, treatment with iodine agents (such as potassium iodide) can effectively inhibit the synthesis of thyroid hormones and inhibit the conversion of T4 to thereby reduce the level of thyroid hormones in the blood circulation
    .

    It starts to work within 24 hours after administration
    .

    Preoperative iodine treatment for 8-10 days can reduce the vascular supply of thyroid tissue
    .

    Iodine treatment needs to last for 2 weeks to achieve the maximum therapeutic effect
    .

    Before using iodine treatment, antithyroid drugs must be used to restore thyroid function to normal, otherwise exogenous iodide can be used as a substrate to participate in the synthesis of new thyroid hormones
    .

    Exogenous iodine destroys the function of thyroid cells and inhibits the combination of endogenous iodine
    .

    This Wolff-Chaikoff effect lasts only a few days
    .

    After that, although iodine continued to be ingested in large quantities, thyroid hormones began to be synthesized again
    .

    Therefore, iodine therapy is suitable for patients with hyperthyroidism in crisis and those who need emergency surgery
    .

    Iodine therapy is forbidden for children, pregnant women, and breastfeeding women.
    It has been reported that it is safe to stop the drug for 4 months or more before pregnancy
    .

    Beta blockers are used to block the peripheral adrenergic effects of hyperthyroidism
    .

    After medication, the patient's clinical symptoms can return to normal, but if no other treatment is added, the patient's laboratory test results still show hyperthyroidism
    .

    Propranolol can also reduce the conversion of T4 to T3 in peripheral tissues, so it is the most commonly used β-adrenergic receptor antagonist in the treatment of hyperthyroidism
    .

    Patients with thyrotoxicosis may require larger doses of beta blockers due to increased metabolism
    .

    Centrally acting adrenergic antagonists such as reserpine and calcium channel blockers such as diltiazem can be used for patients who cannot be treated with beta blockers
    .

    B6.
    What are the benefits of adrenergic block? Catecholamines are related to the symptoms of thyrotoxicosis
    .

    Drugs that can reduce the storage of catecholamines or block the effects of catecholamines
    .

    It can lower the heart rate, reduce cardiac output, and reduce the excitability of the heart
    .

    The drugs used to treat the symptoms of thyroid toxicity include: β-blockers, α-β-blockers, and centrally acting adrenergic antagonists such as reserpine
    .

    The use of these drugs may have the following related side effects: hypotension, sedation, depression, myocardial depression, bronchospasm, and diarrhea
    .

    B7.
    When can patients with hyperthyroidism undergo elective surgery? The patient's treatment should focus on relieving symptoms
    .

    The patient should return to normal heart rate, pulse pressure and sinus rhythm, and the recent cardiac murmur disappeared
    .

    Symptoms such as tremor, anxiety, palpitations, and heat intolerance should be relieved
    .

    B8.
    How do patients with hyperthyroidism give preoperative medication? The purpose of preoperative medication for patients with thyrotoxicosis is to relieve anxiety and prevent sympathetic nervous system excitement
    .

    Preoperative medications often use benzodiazepines such as diazepam (5-20mg orally) or central adrenergic inhibitors such as clonidine (3~5ug/kg orally)
    .

    Because antimuscarinic drugs such as atropine and scopolamine can cause tachycardia and interfere with normal body temperature regulation, their use is not recommended
    .

    B9.
    How to prepare before surgery for patients with thyrotoxicosis undergoing emergency surgery? When a patient needs emergency surgery, measures need to be taken to prevent a hyperthyroid crisis
    .

    Try to use propranolol to reduce the high adrenergic state and reduce the conversion of T4 to T3
    .

    Esmolol can also be used due to its β1 receptor specificity and short half-life
    .

    But esmolol cannot reduce the conversion of T4 to T3 in peripheral tissues
    .

    Antithyroid drugs should also be given to prevent further synthesis of thyroid hormones
    .

    Give as early as possible oral propylthiouracil 200-400 mg every 6 hours or oral methimazole 20-40 mg every 6 hours
    .

    Methimazole dissolved in an aqueous solution can be used for rectal administration, but propylthiouracil cannot
    .

    Both propylthiouracil and glucocorticoid can inhibit the conversion of T4 to T3 in peripheral tissues, and the combination of the two drugs can have a synergistic effect
    .

    Dexamethasone (2 mg every 6 hours) or hydrocortisone (40 mg every 6 hours) can be given intravenously.
    Potassium iodide saturated solution (5 drops orally every 6 hours) or Lugo's solution (30 drops every 6 to 8 hours) After administration, the release of T4 and T3 can be quickly inhibited
    .

    Anti-parasympathetic drugs such as atropine and pancuronium should be avoided because they can relatively enhance the activity of the sympathetic nervous system
    .

    Treatment should also pay attention to correct systemic decompensation
    .

    Liquid and electrolyte need to be adjusted to normal
    .

    If low blood pressure occurs, and infusion alone cannot be corrected, invasive monitoring is necessary to guide the use of inotropic drugs and vasopressors
    .

    If you want to know what is going on, let’s look at the next breakdown of the notes of the Luffy Medical Channel
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